The present invention relates to medical devices, and in particular, to methods, devices, and systems for controlling contraction of a heart. During a normal heart beat, the heart contracts in a coordinated fashion to pump blood. In particular, the heart contracts based on rhythmic electrical impulses, which are spread over the heart using specialized fibers. These rhythmic electrical pulses are initiated by the heart's natural pacemaker called the sino-atrial node (SA node). In a normal heart there is a main pathway for the electrical current, which passes from the upper part of the heart (the atria) to the lower part (the ventricles). First, the SA node initiates electrical impulses to cause the right and left atria to contract. As the atria contract, the electrical impulses from the SA node propagate to the atrial-ventricular node (“AV node”). The time these impulses take to propagate from the SA node through the AV node is known as the A-V delay. The A-V delay allows the atria to fully contract and fill the ventricles with blood. The AV node then transmits a second impulse, which causes contraction in the right and left ventricles. Blood from the ventricles then flows out of the heart and to the rest of the body. Therefore, the heart relies upon a rhythmic cycle of electrical impulses to pump blood efficiently.
A heart, however, may have cardiac defects that interfere with the rhythmic cycle or conduction of electrical impulses. For example, there are types of cardiac deficiencies that cause early stimulation and contraction in the heart. Such pre-excitation deficiencies exist, for example, where the ventricles are activated by the impulse originating from the atrium at a time earlier than would be expected if the impulse reached the ventricles by way of the normal conduction system described above. For example, the Wolff-Parkinson-White syndrome is characterized by early stimulation and contraction of the ventricles. In Wolff-Parkinson-White syndrome, there is an accessory conducting pathway that leads from the atria to the ventricles. This pathway may at times encourage a rapid rhythm. In particular, instead of allowing the next heart beat to begin at the SA node, the extra pathway can pick up an electrical impulse in the ventricles and send it back upward to the atria. When this happens, the impulse begins to travel abnormally in a rapid, circular manner, causing a rapid heart rate.
As noted above, a normal heartbeat includes an optimum A-V delay period to allow the atria to fully contract and fill the ventricles with blood. Cardiac defects, such as Wolff-Parkinson-White, cause early stimulation and contraction of the ventricles before the end of the A-V delay period, and thus, decrease the efficiency of the heart and may lead to heart failure.
Unfortunately, known stimulation devices, such as artificial pacemakers, cannot compensate for such early stimulation in the heart. While Wolff-Parkinson-White syndrome may be controlled by certain drugs or through a procedure known as catheter ablation, known implantable devices only apply stimulating pulses to assist contraction in the heart and are unable to compensate for early stimulation, such as in Wolff-Parkinson-White syndrome. Accordingly, it would be desirable to provide methods, apparatus, and systems, which can overcome these and other deficiencies in the prior art, for example, to assist the heart in contracting in a coordinated fashion.